Regulatory networks of senescence-associated gene-transcription factors promote degradation in Moso bamboo shoots.
Wenyu ZhangMan ShiKebin YangJunbo ZhangZhimin GaoYousry A El-KassabyQuan LiTingting CaoShixin DengHongsheng QingZhikang WangXinzhang SongPublished in: Plant, cell & environment (2024)
Bamboo cultivation, particularly Moso bamboo (Phyllostachys edulis), holds significant economic importance in various regions worldwide. Bamboo shoot degradation (BSD) severely affects productivity and economic viability. However, despite its agricultural consequences, the molecular mechanisms underlying BSD remain unclear. Consequently, we explored the dynamic changes of BSD through anatomy, physiology and the transcriptome. Our findings reveal ruptured protoxylem cells, reduced cell wall thickness and the accumulation of sucrose and reactive oxygen species (ROS) during BSD. Transcriptomic analysis underscored the importance of genes related to plant hormone signal transduction, sugar metabolism and ROS homoeostasis in this process. Furthermore, BSD appears to be driven by the coexpression regulatory network of senescence-associated gene transcription factors (SAG-TFs), specifically PeSAG39, PeWRKY22 and PeWRKY75, primarily located in the protoxylem of vascular bundles. Yeast one-hybrid and dual-luciferase assays demonstrated that PeWRKY22 and PeWRKY75 activate PeSAG39 expression by binding to its promoter. This study advanced our understanding of the molecular regulatory mechanisms governing BSD, offering a valuable reference for enhancing Moso bamboo forest productivity.
Keyphrases
- genome wide identification
- transcription factor
- cell wall
- reactive oxygen species
- climate change
- dna damage
- dna binding
- genome wide
- cell death
- endothelial cells
- induced apoptosis
- single cell
- high throughput
- cell cycle arrest
- signaling pathway
- stress induced
- optical coherence tomography
- human health
- endoplasmic reticulum stress
- subarachnoid hemorrhage
- brain injury
- binding protein
- life cycle
- pi k akt